Article

Effects of inflammation on bone: An update

University of California, Department of Medicine, San Francisco VA Medical Center, San Francisco, CA, USA
Current opinion in rheumatology (Impact Factor: 5.07). 07/2011; 23(4):389-95. DOI: 10.1097/BOR.0b013e3283474dbe
Source: PubMed

ABSTRACT To present an updated summary of the relationship between inflammation and localized and generalized bone loss in the rheumatic diseases.
In addition to the well established role of inflammatory cytokines in promoting enhanced osteoclast function and bone loss, recent work has discovered the cytokine milieu may also inhibit osteoblast function and bone repair. The WNT and bone morphogenetic protein pathways provide molecular links between inflammation and altered bone homeostasis in chronic inflammatory states. These pathways and others have been the targets of emerging therapies for the management of inflammatory bone loss.
Inflammation and bone loss are linked through a number of molecular pathways. Both of these processes need to be addressed when designing an effective treatment strategy for the rheumatic diseases.

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    • "Of particular note is Wnt/β-catenin signaling, which is necessary and sufficient for caudal fin regeneration (Kawakami et al., 2006; Stoick-Cooper et al., 2007a,b). Given the crucial role of Wnt/β-catenin signaling in zebrafish fin regeneration, as well as evidence that this pathway regulates macrophage chemotaxis, recruitment and inflammatory diseases in several mammalian models (Newman and Hughes, 2012; Matzelle et al., 2012; Baker-LePain et al., 2011; Whyte et al., 2012), Wnt/β-catenin signaling is a candidate for linking inflammation and regeneration in zebrafish. However, it is still relatively unclear how this key pathway is activated and how Wnt/β-catenin signaling affects specific cells and stages of the regenerative process. "
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    Development 07/2014; 141(13):2581-91. DOI:10.1242/dev.098459 · 6.27 Impact Factor
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    • "Chronic inflammation is known to mediate bone loss in a variety of conditions including rheumatoid arthritis and aging [1] [2] [3] [4]. The joint space in rheumatoid arthritis represents the more severe end of the inflammation spectrum where tumor necrosis factor-α (TNF-α) has been shown to promote an inflammatory response, increase expression of receptor activator of nuclear factor kappa-B ligand (RANKL) and osteoclastic resorption [5] [6]. Indeed, therapeutic intervention with anti-TNF drugs retards disease progression [7] [8] [9]. "
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    • "The cytokine milieu determines the effects of inflammation on bone. There is extensive research on the role of proinflammatory cytokines in bone homeostasis (23–25). Blockade of the inflammatory cytokines results in the control of chronic inflammation as well as in protective effects on bone. "
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